The DOI matches its Crossref record; 144 of the 145 references it cites were found in a registry or an index.
Glutaminolysis and autophagy in cancer
Open accessAbstract
The remarkable metabolic differences between cancer cells and normal cells result in the potential for targeted cancer therapy. The upregulation of glutaminolysis provides energetic advantages to cancer cells. The recently described link between glutaminolysis and autophagy, mediated by MTORC1, may constitute an attractive target for therapeutic strategies. A combination of therapies targeting simultane-ously cell signaling, cancer metabolism, and autophagy can solve therapy resistance and tumor relapse problems, commonly observed in patients treated with most of the current targeted therapies. In this review we summarize the mechanistic link between glutaminolysis and autophagy, and discuss the impacts of these processes on cancer progression and the potential for therapeutic intervention.
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“Therefore, enhanced glutaminolysis might eventually contribute to the initiation and progression of cancer by stimulating cell growth via the mTORC1 pathway and enhancing aerobic glycolysis while disrupting the proper elimination of misfolded proteins, damaged DNA and organelles through the inhibition of autophagy and the DNA damage response166.”
From Glutamine reliance in cell metabolism (2020) · cites this paper as [166]
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Glutamine reliance in cell metabolism
Yoo, H. C., Yu, Y. C., Sung, Y., & Han, J. M. (2020) · Experimental & Molecular Medicine · doi:10.1038/s12276-020-00504-8 · Cited by 1,021
Molecular mechanisms of ferroptosis and its role in cancer therapy
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Cancer-associated adipocytes: key players in breast cancer progression
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Metadata
- Authors
- Villar, V. H., Merhi, F., Djavaheri-Mergny, M., & Durán, R. V.
- Affiliations
- Université de Bordeaux (FR)
- INSERM U916 VINCO; Institut Bergonié; Bordeaux, France
- Corresponding author
- Durán, Raúl V
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2015-08-03
- Volume
- 11
- Issue
- 8
- Pages
- 1198-1208
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- PMC
- PMC4590661
- OpenAlex
- W1768966319
- Cited by
- 143
- References
- 145
- Citations by year
- 2026: 6 · 2025: 15 · 2024: 14 · 2023: 9 · 2022: 18 · 2021: 18 · 2020: 18 · 2019: 12 · 2018: 15 · 2017: 12 · 2016: 5 · 2015: 1
- FWCI
- 1.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Autophagy (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Institut National de la Santé et de la Recherche Médicale
- Fondation ARC pour la Recherche sur le Cancer
- Ligue Contre le Cancer
- Institut National Du Cancer
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Keywords
- glutaminolysis, cancer metabolism, mTORC1 signaling, cancer cell energy metabolism, targeted cancer therapy, treatment resistance, tumor recurrence, tumor progression
- MeSH terms
- Mechanistic Target of Rapamycin Complex 1, Animals, Autophagy, Cell Transformation, Neoplastic, Glutamine, Humans, Ketoglutaric Acids, Neoplasm Recurrence, Local, Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Reactive Oxygen Species, Drug Resistance, Neoplasm, Multiprotein Complexes, Cell Proliferation, TOR Serine-Threonine Kinases
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